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Journal articles on the topic 'Dopaminergic mechanisms'

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Published: 4 June 2021
Last updated: 30 July 2024

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1

Millichap, J. Gordon, and John J. Millichap. "Dopaminergic Mechanisms in Adhd." Pediatric Neurology Briefs 28, no. 1 (January 1, 2014): 8. http://dx.doi.org/10.15844/pedneurbriefs-28-1-10.

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2

Razzolini, R., P. Ostan, A. Ramondo, P. Stritoni, R. Chioin, and S. Dalla-Volta. "Dopaminergic mechanisms in heart failure." Pharmacological Research 22 (September 1990): 422. http://dx.doi.org/10.1016/s1043-6618(09)80432-5.

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3

Barone, P., K. S. Bankiewicz, G. U. Corsini, I. J. Kopin, and T. N. Chase. "Dopaminergic mechanisms in hemiparkinsonian monkeys." Neurology 37, no. 10 (October 1, 1987): 1592. http://dx.doi.org/10.1212/wnl.37.10.1592.

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4

IMAM, SYED Z. "Molecular Mechanisms of Dopaminergic Neurodegeneration." Annals of the New York Academy of Sciences 993, no. 1 (May 2003): 377. http://dx.doi.org/10.1111/j.1749-6632.2003.tb07547.x.

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5

Chen, Jianping. "Dopaminergic mechanisms and brain reward." Seminars in Neuroscience 5, no. 5 (October 1993): 315–20. http://dx.doi.org/10.1016/s1044-5765(05)80038-7.

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6

Lu, Jing-Shan, Qi-Yu Chen, Xiang Chen, Xu-Hui Li, Zhaoxiang Zhou, Qin Liu, Yuwan Lin, Miaomiao Zhou, Ping-Yi Xu, and Min Zhuo. "Cellular and synaptic mechanisms for Parkinson’s disease-related chronic pain." Molecular Pain 17 (January 2021): 174480692199902. http://dx.doi.org/10.1177/1744806921999025.

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Parkinson’s disease is the second most common neurodegenerative disorder after Alzheimer’s disease. Chronic pain is experienced by the vast majority of patients living with Parkinson’s disease. The degeneration of dopaminergic neuron acts as the essential mechanism of Parkinson’s disease in the midbrain dopaminergic pathway. The impairment of dopaminergic neurons leads to dysfunctions of the nociceptive system. Key cortical areas, such as the anterior cingulate cortex (ACC) and insular cortex (IC) that receive the dopaminergic projections are involved in pain transmission. Dopamine changes synaptic transmission via several pathway, for example the D2-adenly cyclase (AC)-cyclic AMP (cAMP)-protein kinase A (PKA) pathway and D1-G protein-coupled receptor kinase 2 (GRK2)-fragile X mental retardation protein (FMRP) pathway. The management of Parkinson’s disease-related pain implicates maintenance of stable level of dopaminergic drugs and analgesics, however a more selective drug targeting at key molecules in Parkinson’s disease-related pain remains to be investigated.
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7

Hughes, A., G. Martin, S. Thom, and P. Sever. "Dopaminergic Mechanisms in Human Peripheral Vasculature." Journal of Hypertension 3, no. 6 (December 1985): 664–65. http://dx.doi.org/10.1097/00004872-198512000-00024.

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8

Wood, Patrick B. "Mesolimbic dopaminergic mechanisms and pain control." Pain 120, no. 3 (February 2006): 230–34. http://dx.doi.org/10.1016/j.pain.2005.12.014.

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9

Riddle, Evan L., Annette E. Fleckenstein, and Glen R. Hanson. "Mechanisms of methamphetamine-induced dopaminergic neurotoxicity." AAPS Journal 8, no. 2 (June 2006): E413—E418. http://dx.doi.org/10.1007/bf02854914.

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10

Wickens, J. R., J. C. Horvitz, R. M. Costa, and S. Killcross. "Dopaminergic Mechanisms in Actions and Habits." Journal of Neuroscience 27, no. 31 (August 1, 2007): 8181–83. http://dx.doi.org/10.1523/jneurosci.1671-07.2007.

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11

Meltzer, Herbert Y. "Clozapine Withdrawal: Serotonergic or Dopaminergic Mechanisms?" Archives of General Psychiatry 54, no. 8 (August 1, 1997): 760. http://dx.doi.org/10.1001/archpsyc.1997.01830200094013.

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12

Wasel, Ola, and Jennifer L. Freeman. "Chemical and Genetic Zebrafish Models to Define Mechanisms of and Treatments for Dopaminergic Neurodegeneration." International Journal of Molecular Sciences 21, no. 17 (August 20, 2020): 5981. http://dx.doi.org/10.3390/ijms21175981.

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The zebrafish (Danio rerio) is routinely used in biological studies as a vertebrate model system that provides unique strengths allowing applications in studies of neurodevelopmental and neurodegenerative diseases. One specific advantage is that the neurotransmitter systems are highly conserved throughout vertebrate evolution, including between zebrafish and humans. Disruption of the dopaminergic signaling pathway is linked to multiple neurological disorders. One of the most common is Parkinson’s disease, a neurodegenerative disease associated with the loss of dopaminergic neurons, among other neuropathological characteristics. In this review, the development of the zebrafish’s dopaminergic system, focusing on genetic control of the dopaminergic system, is detailed. Second, neurotoxicant models used to study dopaminergic neuronal loss, including 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), the pesticides paraquat and rotenone, and 6-hydroxydopamine (6-OHDA), are described. Next, zebrafish genetic knockdown models of dj1, pink1, and prkn established for investigating mechanisms of Parkinson’s disease are discussed. Chemical modulators of the dopaminergic system are also highlighted to showcase the applicability of the zebrafish to identify mechanisms and treatments for neurodegenerative diseases such as Parkinson’s disease associated with the dopaminergic system.
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13

Kolomentsev, S. V., A. V. Kolomentseva, I. V. Litvinenko, P. A. Polezhaev, M. S. Yaroslavtseva, A. A. Kirpichenko, and A. V. Ryabtsev. "Dopamine antinociceptive system." Vestnik nevrologii, psihiatrii i nejrohirurgii (Bulletin of Neurology, Psychiatry and Neurosurgery), no. 11 (November 27, 2023): 878–90. http://dx.doi.org/10.33920/med-01-2311-03.

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The article presents modern views on structure and functioning of dopaminergic structures of the brain and spinal cord and their role in mechanisms of antinociception, formation, and chronification of different pain syndrome types. The paper provides a detailed description of analgesic effects of various dopamine receptors in the structures of the CNS (the spinal cord, ventral tegmental area, periaqueductal gray, corpus striatum, nucleus accumbens, hypothalamus, and medial prefrontal cortex) which function as the dopaminergic antinociceptive system. The results of numerous investigations carried out on models of neuropathic pain syndrome have shown that D2 dopamine receptors possess the greatest analgesic activity. Their antinociceptive mechanism of action is effectuated at the level of substantia gelatinosa of the spinal cord and cerebral dopaminergic structures. D1‑like receptors have lower analgesic activity and different mechanisms of action depending on localization within the brain. High availability of D2/D3 receptors in corpus striatum is indicative of a low synaptic level of endogenous dopamine and leads to reduction of pain perception threshold. On the contrary, low availability of D2/D3 receptors results in the increase of pain perception threshold. The dopaminergic antinociceptive system is characterized by a modulating effect on other neurotransmitter systems participating in nociception and antinociception. An important mechanism of antinociception of dopaminergic structures is connected with superadditivity and synergism of D2 receptors with opioid receptors. Proven participation of dopaminergic structures in pain perception and analgesia demonstrates a potential possible application of D2‑receptors agonists as an adjuvant method for achieving a greater effect in therapeutic multimodal schemes of analgesia.
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14

Vasile, Titus Mihai, and Ovidiu Bajenaru. "Dopaminergic and non-dopaminergic mechanisms of non-motor symptoms of Parkinson disease." Romanian Journal of Neurology 11, no. 4 (December 31, 2012): 158–64. http://dx.doi.org/10.37897/rjn.2012.4.2.

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During the last years, the non-motor aspects of Parkinson’s disease were in the focus of the attention in Movement Disorders Society and experts. Some clinical and research instruments like NMSS (Non-Motor Symptoms Scale) help clinicians to recognize and evaluate these aspects that are common and occur across all stages of PD. Some non-motor symptoms like sleep problems, autonomic dysfunction and pain are partly dopaminergic but others are non-dopaminergic. When they are treatable, the treatment can increase the quality of life for these patients.
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15

Kim, Sanghoon, Edward Pajarillo, Ivan Nyarko-Danquah, Michael Aschner, and Eunsook Lee. "Role of Astrocytes in Parkinson’s Disease Associated with Genetic Mutations and Neurotoxicants." Cells 12, no. 4 (February 15, 2023): 622. http://dx.doi.org/10.3390/cells12040622.

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Parkinson’s disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons and the aggregation of Lewy bodies in the basal ganglia, resulting in movement impairment referred to as parkinsonism. However, the etiology of PD is not well known, with genetic factors accounting only for 10–15% of all PD cases. The pathogenetic mechanism of PD is not completely understood, although several mechanisms, such as oxidative stress and inflammation, have been suggested. Understanding the mechanisms of PD pathogenesis is critical for developing highly efficacious therapeutics. In the PD brain, dopaminergic neurons degenerate mainly in the basal ganglia, but recently emerging evidence has shown that astrocytes also significantly contribute to dopaminergic neuronal death. In this review, we discuss the role of astrocytes in PD pathogenesis due to mutations in α-synuclein (PARK1), DJ-1 (PARK7), parkin (PARK2), leucine-rich repeat kinase 2 (LRRK2, PARK8), and PTEN-induced kinase 1 (PINK1, PARK6). We also discuss PD experimental models using neurotoxins, such as paraquat, rotenone, 6-hydroxydopamine, and MPTP/MPP+. A more precise and comprehensive understanding of astrocytes’ modulatory roles in dopaminergic neurodegeneration in PD will help develop novel strategies for effective PD therapeutics.
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16

Baldessarini, Ross J. "Clozapine Withdrawal: Serotonergic or Dopaminergic Mechanisms?-Reply." Archives of General Psychiatry 54, no. 8 (August 1, 1997): 761. http://dx.doi.org/10.1001/archpsyc.1997.01830200095014.

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17

Seeman, Philip. "Clozapine Withdrawal: Serotonergic or Dopaminergic Mechanisms?-Reply." Archives of General Psychiatry 54, no. 8 (August 1, 1997): 762. http://dx.doi.org/10.1001/archpsyc.1997.01830200096015.

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18

Ogawa, Teruyuki, Satoshi Seki, Hitoshi Masuda, Yasuhiko Igawa, Osamu Nishizawa, Sadako Kuno, Michael B. Chancellor, William C. de Groat, and Naoki Yoshimura. "Dopaminergic mechanisms controlling urethral function in rats." Neurourology and Urodynamics 25, no. 5 (2006): 480–89. http://dx.doi.org/10.1002/nau.20260.

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19

Magalingam, Kasthuri Bai, Ammu Kutty Radhakrishnan, and Nagaraja Haleagrahara. "Protective Mechanisms of Flavonoids in Parkinson’s Disease." Oxidative Medicine and Cellular Longevity 2015 (2015): 1–14. http://dx.doi.org/10.1155/2015/314560.

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Parkinson’s disease is a chronic, debilitating neurodegenerative movement disorder characterized by progressive degeneration of dopaminergic neurons in thesubstantia nigra pars compactaregion in human midbrain. To date, oxidative stress is the well accepted concept in the etiology and progression of Parkinson’s disease. Hence, the therapeutic agent is targeted against suppressing and alleviating the oxidative stress-induced cellular damage. Within the past decades, an explosion of research discoveries has reported on the protective mechanisms of flavonoids, which are plant-based polyphenols, in the treatment of neurodegenerative disease using bothin vitroandin vivomodels. In this paper, we have reviewed the literature on the neuroprotective mechanisms of flavonoids in protecting the dopaminergic neurons hence reducing the symptoms of this movement disorder. The mechanism reviewed includes effect of flavonoids in activation of endogenous antioxidant enzymes, suppressing the lipid peroxidation, inhibition of inflammatory mediators, flavonoids as a mitochondrial target therapy, and modulation of gene expression in neuronal cells.
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20

Sakurada, K., M. Ohshima-Sakurada, T. D. Palmer, and F. H. Gage. "Nurr1, an orphan nuclear receptor, is a transcriptional activator of endogenous tyrosine hydroxylase in neural progenitor cells derived from the adult brain." Development 126, no. 18 (September 15, 1999): 4017–26. http://dx.doi.org/10.1242/dev.126.18.4017.

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Adult rat-derived hippocampal progenitor cells express many of the molecules implicated in midbrain dopaminergic determination, including FGF receptors 1, 2 and 3, the sonic hedgehog receptor components Smo and Ptc, and the region-specific transcription factors Ptx3 and Nurr1. Here we use undifferentiated progenitors to probe the events leading to the dopaminergic phenotype and find that the influences of Nurr1 can be temporally and mechanistically uncoupled from the patterning influences of sonic hedgehog and FGF-8 or the more generic process of neuronal differentiation itself. In gain-of-function experiments, Nurr1 is able to activate transcription of the tyrosine hydroxylase gene by binding a response element within a region of the tyrosine hydroxylase promoter necessary for midbrain-specific expression. This activation is mediated through a retinoid X receptor independent mechanism and occurs in all precursors, regardless of differentiation status. Overexpression of Nurr1 does not affect proliferation or stimulate neuronal differentiation and has no influence on the expression of other dopaminergic markers. This uncoupling of tyrosine hydroxylase expression from other dopaminergic markers suggests that the midbrain dopaminergic identity is dictated by a combination of pan-dopaminergic (e.g., Shh/FGF-8) and region-specific (Nurr1) mechanisms.
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21

Kweon, Gi-Ryang, Jeremy D. Marks, Robert Krencik, Eric H. Leung, Paul T. Schumacker, Keith Hyland, and Un Jung Kang. "Distinct Mechanisms of Neurodegeneration Induced by Chronic Complex I Inhibition in Dopaminergic and Non-dopaminergic Cells." Journal of Biological Chemistry 279, no. 50 (October 6, 2004): 51783–92. http://dx.doi.org/10.1074/jbc.m407336200.

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Chronic mitochondrial dysfunction, in particular of complex I, has been strongly implicated in the dopaminergic neurodegeneration in Parkinson's disease. To elucidate the mechanisms of chronic complex I disruption-induced neurodegeneration, we induced differentiation of immortalized midbrain dopaminergic (MN9D) and non-dopaminergic (MN9X) neuronal cells, to maintain them in culture without significant cell proliferation and compared their survivals following chronic exposure to nanomolar rotenone, an irreversible complex I inhibitor. Rotenone killed more dopaminergic MN9D cells than non-dopaminergic MN9X cells. Oxidative stress played an important role in rotenone-induced neurodegeneration of MN9X cells, but not MN9D cells: rotenone oxidatively modified proteins more in MN9X cells than in MN9D cells and antioxidants decreased rotenone toxicity only in MN9X cells. MN9X cells were also more sensitive to exogenous oxidants than MN9D cells. In contrast, disruption of bioenergetics played a more important role in MN9D cells: rotenone decreased mitochondrial membrane protential and ATP levels in MN9D cells more than in MN9X cells. Supplementation of cellular energy with a ketone body,d-β-hydroxybutyrate, decreased rotenone toxicity in MN9D cells, but not in MN9X cells. MN9D cells were also more susceptible to disruption of oxidative phosphorylation or glycolysis than MN9X cells. These findings indicate that, during chronic rotenone exposure, MN9D cells die primarily through mitochondrial energy disruption, whereas MN9X cells die primarily via oxidative stress. Thus, intrinsic properties of individual cell types play important roles in determining the predominant mechanism of complex I inhibition-induced neurodegeneration.
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22

Zhao, Yadan, Zichen Zhang, Siru Qin, Wen Fan, Wei Li, Jingyi Liu, Songtao Wang, Zhifang Xu, and Meidan Zhao. "Acupuncture for Parkinson’s Disease: Efficacy Evaluation and Mechanisms in the Dopaminergic Neural Circuit." Neural Plasticity 2021 (June 15, 2021): 1–23. http://dx.doi.org/10.1155/2021/9926445.

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Parkinson’s disease (PD) is a chronic and progressive neurodegenerative disease caused by degeneration of dopaminergic neurons in the substantia nigra. Existing pharmaceutical treatments offer alleviation of symptoms but cannot delay disease progression and are often associated with significant side effects. Clinical studies have demonstrated that acupuncture may be beneficial for PD treatment, particularly in terms of ameliorating PD symptoms when combined with anti-PD medication, reducing the required dose of medication and associated side effects. During early stages of PD, acupuncture may even be used to replace medication. It has also been found that acupuncture can protect dopaminergic neurons from degeneration via antioxidative stress, anti-inflammatory, and antiapoptotic pathways as well as modulating the neurotransmitter balance in the basal ganglia circuit. Here, we review current studies and reflect on the potential of acupuncture as a novel and effective treatment strategy for PD. We found that particularly during the early stages, acupuncture may reduce neurodegeneration of dopaminergic neurons and regulate the balance of the dopaminergic circuit, thus delaying the progression of the disease. The benefits of acupuncture will need to be further verified through basic and clinical studies.
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23

Ruiz-Pozo, Viviana A., Rafael Tamayo-Trujillo, Santiago Cadena-Ullauri, Evelyn Frias-Toral, Patricia Guevara-Ramírez, Elius Paz-Cruz, Sebastián Chapela, et al. "The Molecular Mechanisms of the Relationship between Insulin Resistance and Parkinson’s Disease Pathogenesis." Nutrients 15, no. 16 (August 15, 2023): 3585. http://dx.doi.org/10.3390/nu15163585.

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Parkinson’s disease (PD) is a degenerative condition resulting from the loss of dopaminergic neurons. This neuronal loss leads to motor and non-motor neurological symptoms. Most PD cases are idiopathic, and no cure is available. Recently, it has been proposed that insulin resistance (IR) could be a central factor in PD development. IR has been associated with PD neuropathological features like α-synuclein aggregation, dopaminergic neuronal loss, neuroinflammation, mitochondrial dysfunction, and autophagy. These features are related to impaired neurological metabolism, neuronal death, and the aggravation of PD symptoms. Moreover, pharmacological options that involve insulin signaling improvement and dopaminergic and non-dopaminergic strategies have been under development. These drugs could prevent the metabolic pathways involved in neuronal damage. All these approaches could improve PD outcomes. Also, new biomarker identification may allow for an earlier PD diagnosis in high-risk individuals. This review describes the main pathways implicated in PD development involving IR. Also, it presents several therapeutic options that are directed at insulin signaling improvement and could be used in PD treatment. The understanding of IR molecular mechanisms involved in neurodegenerative development could enhance PD therapeutic options and diagnosis.
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24

Thorn, Catherine. "Dopaminergic mechanisms of VNS-induced motor system plasticity." Brain Stimulation 14, no. 6 (November 2021): 1709–10. http://dx.doi.org/10.1016/j.brs.2021.10.398.

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25

Lévesque, Martin. "Mechanisms controlling the diversity of dopaminergic axon projections." Intrinsic Activity 4, Suppl. 2 (August 29, 2016): A2.2. http://dx.doi.org/10.25006/ia.4.s2-a2.2.

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26

Mello-Carpes, Pâmela Billig, Niége Alves, Liane da Silva de Vargas, and Karine Ramires Lima. "Novelty Exposition Facilitates Memory Extinction By Dopaminergic Mechanisms." FASEB Journal 34, S1 (April 2020): 1. http://dx.doi.org/10.1096/fasebj.2020.34.s1.02965.

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27

Goldstein, Menek, and Ariel Y. Deutch. "Dopaminergic mechanisms in the pathogenesis of schizophrenia 1." FASEB Journal 6, no. 7 (April 1992): 2413–21. http://dx.doi.org/10.1096/fasebj.6.7.1348713.

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28

Subramaniyan, Manivannan, and John A. Dani. "Dopaminergic and cholinergic learning mechanisms in nicotine addiction." Annals of the New York Academy of Sciences 1349, no. 1 (August 24, 2015): 46–63. http://dx.doi.org/10.1111/nyas.12871.

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29

Jadhav, Arun L. "Low level lead exposure and central dopaminergic mechanisms." Toxicology Letters 95 (July 1998): 127. http://dx.doi.org/10.1016/s0378-4274(98)80504-3.

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30

Porcelli, S., A. Drago, C. Fabbri, and A. Serretti. "Mechanisms of antidepressant action: An integrated dopaminergic perspective." Progress in Neuro-Psychopharmacology and Biological Psychiatry 35, no. 7 (August 2011): 1532–43. http://dx.doi.org/10.1016/j.pnpbp.2011.03.005.

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31

Willner, P., R. Muscat, M. Papp, J. Stamford, and Z. Kruk. "Dopaminergic mechanisms in an animal model of anhedonia." European Neuropsychopharmacology 1, no. 3 (September 1991): 295–96. http://dx.doi.org/10.1016/0924-977x(91)90534-2.

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32

Basbaum, A. I., and W. Magerl. "112 Workshop Summary: DOPAMINERGIC MECHANISMS OF PAIN CONTROL." European Journal of Pain 11, S1 (June 2007): S44—S45. http://dx.doi.org/10.1016/j.ejpain.2007.03.126.

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33

Lieberman, J. A., B. J. Kinon, and A. D. Loebel. "Dopaminergic Mechanisms in Idiopathic and Drug-induced Psychoses." Schizophrenia Bulletin 16, no. 1 (January 1, 1990): 97–110. http://dx.doi.org/10.1093/schbul/16.1.97.

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34

Berry, Anne S., Vyoma D. Shah, Suzanne L. Baker, Jacob W. Vogel, James P. O'Neil, Mustafa Janabi, Henry D. Schwimmer, Shawn M. Marks, and William J. Jagust. "Aging Affects Dopaminergic Neural Mechanisms of Cognitive Flexibility." Journal of Neuroscience 36, no. 50 (November 2, 2016): 12559–69. http://dx.doi.org/10.1523/jneurosci.0626-16.2016.

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35

Berry, Anne S., Robert L. White, Daniella J. Furman, Jenna R. Naskolnakorn, Vyoma D. Shah, Mark D'Esposito, and William J. Jagust. "Dopaminergic Mechanisms Underlying Normal Variation in Trait Anxiety." Journal of Neuroscience 39, no. 14 (February 8, 2019): 2735–44. http://dx.doi.org/10.1523/jneurosci.2382-18.2019.

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36

Lin, John C., and Arnon Rosenthal. "Molecular mechanisms controlling the development of dopaminergic neurons." Seminars in Cell & Developmental Biology 14, no. 3 (June 2003): 175–80. http://dx.doi.org/10.1016/s1084-9521(03)00009-0.

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37

Pignalosa, Francesca Chiara, Antonella Desiderio, Paola Mirra, Cecilia Nigro, Giuseppe Perruolo, Luca Ulianich, Pietro Formisano, et al. "Diabetes and Cognitive Impairment: A Role for Glucotoxicity and Dopaminergic Dysfunction." International Journal of Molecular Sciences 22, no. 22 (November 16, 2021): 12366. http://dx.doi.org/10.3390/ijms222212366.

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Diabetes mellitus (DM) is a chronic metabolic disorder characterized by hyperglycemia, responsible for the onset of several long-term complications. Recent evidence suggests that cognitive dysfunction represents an emerging complication of DM, but the underlying molecular mechanisms are still obscure. Dopamine (DA), a neurotransmitter essentially known for its relevance in the regulation of behavior and movement, modulates cognitive function, too. Interestingly, alterations of the dopaminergic system have been observed in DM. This review aims to offer a comprehensive overview of the most relevant experimental results assessing DA’s role in cognitive function, highlighting the presence of dopaminergic dysfunction in DM and supporting a role for glucotoxicity in DM-associated dopaminergic dysfunction and cognitive impairment. Several studies confirm a role for DA in cognition both in animal models and in humans. Similarly, significant alterations of the dopaminergic system have been observed in animal models of experimental diabetes and in diabetic patients, too. Evidence is accumulating that advanced glycation end products (AGEs) and their precursor methylglyoxal (MGO) are associated with cognitive impairment and alterations of the dopaminergic system. Further research is needed to clarify the molecular mechanisms linking DM-associated dopaminergic dysfunction and cognitive impairment and to assess the deleterious impact of glucotoxicity.
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38

Solms, Mark. "Dreaming and REM sleep are controlled by different brain mechanisms." Behavioral and Brain Sciences 23, no. 6 (December 2000): 843–50. http://dx.doi.org/10.1017/s0140525x00003988.

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The paradigmatic assumption that REM sleep is the physiological equivalent of dreaming is in need of fundamental revision. A mounting body of evidence suggests that dreaming and REM sleep are dissociable states, and that dreaming is controlled by forebrain mechanisms. Recent neuropsychological, radiological, and pharmacological findings suggest that the cholinergic brain stem mechanisms that control the REM state can only generate the psychological phenomena of dreaming through the mediation of a second, probably dopaminergic, forebrain mechanism. The latter mechanism (and thus dreaming itself) can also be activated by a variety of nonREM triggers. Dreaming can be manipulated by dopamine agonists and antagonists with no concomitant change in REM frequency, duration, and density. Dreaming can also be induced by focal forebrain stimulation and by complex partial (forebrain) seizures during nonREM sleep, when the involvement of brainstem REM mechanisms is precluded. Likewise, dreaming is obliterated by focal lesions along a specific (probably dopaminergic) forebrain pathway, and these lesions do not have any appreciable effects on REM frequency, duration, and density. These findings suggest that the forebrain mechanism in question is the final common path to dreaming and that the brainstem oscillator that controls the REM state is just one of the many arousal triggers that can activate this forebrain mechanism. The “REM-on” mechanism (like its various NREM equivalents) therefore stands outside the dream process itself, which is mediated by an independent, forebrain “dream-on” mechanism.
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39

Wang, Jinxu, Xiaolei Miao, Yi Sun, Sijie Li, Anshi Wu, and Changwei Wei. "Dopaminergic System in Promoting Recovery from General Anesthesia." Brain Sciences 13, no. 4 (March 24, 2023): 538. http://dx.doi.org/10.3390/brainsci13040538.

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Dopamine is an important neurotransmitter that plays a biological role by binding to dopamine receptors. The dopaminergic system regulates neural activities, such as reward and punishment, memory, motor control, emotion, and sleep–wake. Numerous studies have confirmed that the dopaminergic system has the function of maintaining wakefulness in the body. In recent years, there has been increasing evidence that the sleep–wake cycle in the brain has similar neurobrain network mechanisms to those associated with the loss and recovery of consciousness induced by general anesthesia. With the continuous development and innovation of neurobiological techniques, the dopaminergic system has now been proved to be involved in the emergence from general anesthesia through the modulation of neuronal activity. This article is an overview of the dopaminergic system and the research progress into its role in wakefulness and general anesthesia recovery. It provides a theoretical basis for interpreting the mechanisms regulating consciousness during general anesthesia.
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40

Medan, Violeta, and Thomas Preuss. "Dopaminergic-induced changes in Mauthner cell excitability disrupt prepulse inhibition in the startle circuit of goldfish." Journal of Neurophysiology 106, no. 6 (December 2011): 3195–204. http://dx.doi.org/10.1152/jn.00644.2011.

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Prepulse inhibition (PPI) is a widespread sensorimotor gating phenomenon characterized by a decrease in startle magnitude if a nonstartling stimulus is presented 20–1,000 ms before a startling stimulus. Dopaminergic agonists disrupt behavioral PPI in various animal models. This provides an important neuropharmacological link to schizophrenia patients that typically show PPI deficits at distinct (60 ms) prepulse-pulse intervals. Here, we study time-dependent effects of dopaminergic modulation in the goldfish Mauthner cell (M-cell) startle network, which shows PPI-like behavioral and physiological startle attenuations. The unique experimental accessibility of the M-cell system allows investigating the underlying cellular mechanism with physiological stimuli in vivo. Our results show that the dopaminergic agonist apomorphine (2 mg/kg body wt) reduced synaptic M-cell PPI by 23.6% ( n = 18; P = 0.009) for prepulse-pulse intervals of 50 ms, whereas other intervals showed no reduction. Consistently, application of the dopamine antagonist haloperidol (0.4 mg/kg body wt) restored PPI to control level. Current ramp injections while recording M-cell membrane potential revealed that apomorphine acts through a postsynaptic, time-dependent mechanism by deinactivating a M-cell membrane nonlinearity, effectively increasing input resistance close to threshold. This increase is most pronounced for prepulse-pulse intervals of 50 ms (47.9%, n = 8; P < 0.05) providing a time-dependent, cellular mechanism for dopaminergic disruption of PPI. These results provide, for the first time, direct evidence of dopaminergic modulation of PPI in the elementary startle circuit of vertebrates and reemphasize the potential of characterizing temporal aspects of PPI at the physiological level to understand its underlying mechanisms.
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41

Kent, Clement, and Pavan Agrawal. "Regulation of Social Stress and Neural Degeneration by Activity-Regulated Genes and Epigenetic Mechanisms in Dopaminergic Neurons." Molecular Neurobiology 57, no. 11 (August 3, 2020): 4500–4510. http://dx.doi.org/10.1007/s12035-020-02037-7.

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Abstract Transcriptional and epigenetic regulation of both dopaminergic neurons and their accompanying glial cells is of great interest in the search for therapies for neurodegenerative disorders such as Parkinson’s disease (PD). In this review, we collate transcriptional and epigenetic changes identified in adult Drosophila melanogaster dopaminergic neurons in response to either prolonged social deprivation or social enrichment, and compare them with changes identified in mammalian dopaminergic neurons during normal development, stress, injury, and neurodegeneration. Surprisingly, a small set of activity-regulated genes (ARG) encoding transcription factors, and a specific pattern of epigenetic marks on gene promoters, are conserved in dopaminergic neurons over the long evolutionary period between mammals and insects. In addition to their classical function as immediate early genes to mark acute neuronal activity, these ARG transcription factors are repurposed in both insects and mammals to respond to chronic perturbations such as social enrichment, social stress, nerve injury, and neurodegeneration. We suggest that these ARG transcription factors and epigenetic marks may represent important targets for future therapeutic intervention strategies in various neurodegenerative disorders including PD.
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Tan, Jolene Su Yi, Yin Xia Chao, Olaf Rötzschke, and Eng-King Tan. "New Insights into Immune-Mediated Mechanisms in Parkinson’s Disease." International Journal of Molecular Sciences 21, no. 23 (December 6, 2020): 9302. http://dx.doi.org/10.3390/ijms21239302.

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The immune system has been increasingly recognized as a major contributor in the pathogenesis of Parkinson’s disease (PD). The double-edged nature of the immune system poses a problem in harnessing immunomodulatory therapies to prevent and slow the progression of this debilitating disease. To tackle this conundrum, understanding the mechanisms underlying immune-mediated neuronal death will aid in the identification of neuroprotective strategies to preserve dopaminergic neurons. Specific innate and adaptive immune mediators may directly or indirectly induce dopaminergic neuronal death. Genetic factors, the gut-brain axis and the recent identification of PD-specific T cells may provide novel mechanistic insights on PD pathogenesis. Future studies to address the gaps in the identification of autoantibodies, variability in immunophenotyping studies and the contribution of gut dysbiosis to PD may eventually provide new therapeutic targets for PD.
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43

Zilfyan, Arto, and Stepan Avagyan. "Nicotine-Dependent Risk Of Developing Parkinson’s Disease." NAMJ 17 (2023), no. 1 (2023): 4–13. http://dx.doi.org/10.56936/18290825-2023.17.2-4.

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For the past twenty years, information concerning the relationship between Parkinson’s disease and the use of tobacco products has appeared in highly respected scientific publications. As a whole, these studies were epidemiological. As a rule, these studies showed that individuals who abused tobacco products for many years and quit smoking only in old age had a significantly increased risk of developing Parkinson’s disease. Only a few studies have attempted to identify the structural-functional relationship between the effects of nicotine on the representative brain areas responsible for the onset of Parkinson’s disease. During prolonged tobacco use, nicotine that enters the brain tissue activates the nicotine-dependent acetylcholine receptors localized in dopaminergic neurons, resulting in the release of dopamine. In this study, we attempted to investigate the mechanisms underlying the onset of Parkinson’s disease in individuals who have quit smoking, i.e. under conditions of nicotine withdrawal in the brain.” In our opinion, the “preventive effect” of nicotine on dopaminergic neurons is realized through four interdependent mechanisms: 1. By the receptor mechanism, due to the nicotine-dependent acetylcholine receptors located on dopaminergic neurons, 2. Due to the balanced release and reuptake of dopamine to dopaminergic neurons, 3. Due to prevention of α-synuclein aggregation and fibrillation process, 4. Due to the inhibitory effect of nicotine on the processes of activating the synthesis of aliphatic polyamines in dopaminergic neurons of the corpus striatum and nucleus caudatum. In cases of nicotine “deficiency”, neurodegenerative disorders pathognomonic for Parkinson’s disease can occur in the brain: 1. The exchange of dopamine and aliphatic polyamines in dopaminergic neurons is disturbed, 2. The processes of transforming native α-synuclein into its aggregated and fibrillar forms are intensified, 3. Ultimately, the intraneuronal dopamine-synuclein complex with a pronounced neurotoxic action spectrum may appear. 4. Older adults, in conditions of abrupt smoking cessation, are recommended to use Eflornithine, as well as a polyamine-free and polyamine-deficient diet.
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44

Vanes, Lucy D., Elias Mouchlianitis, Tracy Collier, Bruno B. Averbeck, and Sukhi S. Shergill. "Differential neural reward mechanisms in treatment-responsive and treatment-resistant schizophrenia." Psychological Medicine 48, no. 14 (February 14, 2018): 2418–27. http://dx.doi.org/10.1017/s0033291718000041.

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AbstractBackgroundThe significant proportion of schizophrenia patients refractory to treatment, primarily directed at the dopamine system, suggests that multiple mechanisms may underlie psychotic symptoms. Reinforcement learning tasks have been employed in schizophrenia to assess dopaminergic functioning and reward processing, but these have not directly compared groups of treatment-refractory and non-refractory patients.MethodsIn the current functional magnetic resonance imaging study, 21 patients with treatment-resistant schizophrenia (TRS), 21 patients with non-treatment-resistant schizophrenia (NTR), and 24 healthy controls (HC) performed a probabilistic reinforcement learning task, utilizing emotionally valenced face stimuli which elicit a social bias toward happy faces. Behavior was characterized with a reinforcement learning model. Trial-wise reward prediction error (RPE)-related neural activation and the differential impact of emotional bias on these reward signals were compared between groups.ResultsPatients showed impaired reinforcement learning relative to controls, while all groups demonstrated an emotional bias favoring happy faces. The pattern of RPE signaling was similar in the HC and TRS groups, whereas NTR patients showed significant attenuation of RPE-related activation in striatal, thalamic, precentral, parietal, and cerebellar regions. TRS patients, but not NTR patients, showed a positive relationship between emotional bias and RPE signal during negative feedback in bilateral thalamus and caudate.ConclusionTRS can be dissociated from NTR on the basis of a different neural mechanism underlying reinforcement learning. The data support the hypothesis that a favorable response to antipsychotic treatment is contingent on dopaminergic dysfunction, characterized by aberrant RPE signaling, whereas treatment resistance may be characterized by an abnormality of a non-dopaminergic mechanism – a glutamatergic mechanism would be a possible candidate.
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45

Velásquez, Marienmy del V., Alexander E. Albarracín, Kelvin Boscán, Ligia B. Angel, Rodolfo E. Izquierdo, María M. Ramírez, Biagina del C. Migliore, et al. "Efecto del compuesto N-2,6-dicloro-aralquil-2-Aminoindano en la conducta estereotipada de ratas. Acción dopaminérgica selectiva central sobre los ganglios basales más que en las estructuras límbicas." Investigación Clínica 64, no. 1 (March 3, 2023): 15–27. http://dx.doi.org/10.54817/ic.v64n1a02.

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Dopamine 1 is involved in neurodegenerative disorders affect-ing the central nervous system (CNS), such as Parkinson’s disease. Despite the absence of some available drugs capable of preventing, stopping or curing the progression of such diseases, there are numerous compounds designed, synthesized, and pharmacologically tested which give rise to pharmacophoric generalizations about the dopaminergic receptor required for the search of a drug able to improve or cure those pathologies. N-aralkyl-2-aminoindane de-rivatives have shown selective activity in the central dopaminergic system. Both the N-[(2,4-dichlorophenyl)-1-methyl-ethyl]-2-aminoindane hydrochloride 2and N-[(3,4-dichlorophenyl)-1-methyl-ethyl]-2-aminoindane hydrochloride 3 showed an agonistic activity mediated by central dopaminergic mechanisms. To contribute to the search of new drugs able to re-establish homeostasis in the dopaminergic transmission in Parkinson’s disease, the compound N-2,6-dichloro-aralkyl-2-aminoindane 4 was designed through medicinal chemistry strategies that contain pharmacophoric approximations of prodrugs. The phar-macological evaluation of compound 4 in the stereotyped behavior of male Sprague Dawley rats showed agonistic activity through the activation of central dopaminergic mechanisms and a higher selectivity in the responses of stereo-typed behavior characteristic of the basal ganglia over the typical responses from limbic structures.
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46

McDonald, Kirstin O., Nikita M. A. Lyons, Luca K. C. Gray, Janet B. Xu, Lucia Schoderboeck, Stephanie M. Hughes, and Indranil Basak. "Transcription Factor-Mediated Generation of Dopaminergic Neurons from Human iPSCs—A Comparison of Methods." Cells 13, no. 12 (June 11, 2024): 1016. http://dx.doi.org/10.3390/cells13121016.

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Dopaminergic neurons are the predominant brain cells affected in Parkinson’s disease. With the limited availability of live human brain dopaminergic neurons to study pathological mechanisms of Parkinson’s disease, dopaminergic neurons have been generated from human-skin-cell-derived induced pluripotent stem cells. Originally, induced pluripotent stem-cell-derived dopaminergic neurons were generated using small molecules. These neurons took more than two months to mature. However, the transcription-factor-mediated differentiation of induced pluripotent stem cells has revealed quicker and cheaper methods to generate dopaminergic neurons. In this study, we compared and contrasted three protocols to generate induced pluripotent stem-cell-derived dopaminergic neurons using transcription-factor-mediated directed differentiation. We deviated from the established protocols using lentivirus transduction to stably integrate different transcription factors into the AAVS1 safe harbour locus of induced pluripotent stem cells. We used different media compositions to generate more than 90% of neurons in the culture, out of which more than 85% of the neurons were dopaminergic neurons within three weeks. Therefore, from our comparative study, we reveal that a combination of transcription factors along with small molecule treatment may be required to generate a pure population of human dopaminergic neurons.
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47

Pascale, Emilia, Giuseppina Divisato, Renata Palladino, Margherita Auriemma, Edward Faustine Ngalya, and Massimiliano Caiazzo. "Noncoding RNAs and Midbrain DA Neurons: Novel Molecular Mechanisms and Therapeutic Targets in Health and Disease." Biomolecules 10, no. 9 (September 3, 2020): 1269. http://dx.doi.org/10.3390/biom10091269.

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Midbrain dopamine neurons have crucial functions in motor and emotional control and their degeneration leads to several neurological dysfunctions such as Parkinson’s disease, addiction, depression, schizophrenia, and others. Despite advances in the understanding of specific altered proteins and coding genes, little is known about cumulative changes in the transcriptional landscape of noncoding genes in midbrain dopamine neurons. Noncoding RNAs—specifically microRNAs and long noncoding RNAs—are emerging as crucial post-transcriptional regulators of gene expression in the brain. The identification of noncoding RNA networks underlying all stages of dopamine neuron development and plasticity is an essential step to deeply understand their physiological role and also their involvement in the etiology of dopaminergic diseases. Here, we provide an update about noncoding RNAs involved in dopaminergic development and metabolism, and the related evidence of these biomolecules for applications in potential treatments for dopaminergic neurodegeneration.
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48

Tressler, Charles. "Dopaminergic Mechanisms in Vision (Neurology and Neurobiology: Volume 43)." Ophthalmic Surgery, Lasers and Imaging Retina 20, no. 11 (November 1989): 829. http://dx.doi.org/10.3928/1542-8877-19891101-21.

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49

Bürki, H., J. Alder, and E. Eichenberger. "Effect of Fluperlapine on Dopaminergic Mechanisms in Rat Brain." Pharmacopsychiatry 18, no. 01 (January 1985): 71–72. http://dx.doi.org/10.1055/s-2007-1017316.

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50

SCHNEIDER, LINDA H. "Orosensory Self-Stimulation by Sucrose Involves Brain Dopaminergic Mechanisms." Annals of the New York Academy of Sciences 575, no. 1 The Psychobio (December 1989): 307–20. http://dx.doi.org/10.1111/j.1749-6632.1989.tb53252.x.

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